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Related Experiment Video

Updated: Jul 14, 2026

Hemogenic Reprogramming of Human Fibroblasts by Enforced Expression of Transcription Factors

Hemogenic Reprogramming of Human Fibroblasts by Enforced Expression of Transcription Factors

Published on: November 4, 2019

IGF binding protein-3 regulates hematopoietic stem cell and endothelial precursor cell function during vascular

Kyung-Hee Chang¹, Tailoi Chan-Ling, Evan L McFarland

¹Program in Stem Cell Biology, University of Florida, Gainesville, FL 32610, USA.

Proceedings of the National Academy of Sciences of the United States of America

|June 15, 2007

Summary

Insulin-like growth factor binding protein-3 (IGFBP3) promotes endothelial precursor cell (EPC) function and vascular repair. IGFBP3 protects against hyperoxia-induced damage and neovascularization, suggesting therapeutic potential for ischemic conditions.

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In Vitro Model of Fetal Human Vessel On-chip to Study Developmental Mechanobiology

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Published on: July 28, 2023

Area of Science:

Vascular biology
Stem cell research
Ophthalmology

Background:

Hypoxia-regulated factors play crucial roles in cellular function and adaptation.
Insulin-like growth factor binding protein-3 (IGFBP3) is a hypoxia-regulated factor with potential roles in cell modulation.
Endothelial precursor cells (EPCs) are vital for vascular repair and neovascularization.

Purpose of the Study:

To investigate the role of IGFBP3 in modulating the function of EPCs and other stem cell populations.
To evaluate the therapeutic potential of IGFBP3 in a mouse model of oxygen-induced retinopathy (OIR).

Main Methods:

Exposure of CD34+ EPCs to IGFBP3 in vitro to assess differentiation, migration, and capillary tube formation.
In vivo studies using neonatal mice in an OIR model, administering IGFBP3-expressing plasmid or IGFBP3-transfected hematopoietic stem cells (HSCs).
Assessment of vascular integrity, vasoobliteration, and neovascularization in the OIR model.

Main Results:

IGFBP3 exposure induced rapid EPC differentiation into endothelial cells, increased cell migration, and enhanced capillary tube formation in vitro.
In the OIR model, both IGFBP3 plasmid and IGFBP3-transfected HSCs significantly reduced vasoobliteration and preretinal neovascularization.
IGFBP3 administration protected the developing vasculature from hyperoxia-induced regression.

Conclusions:

IGFBP3 effectively mediates EPC migration, differentiation, and capillary formation.
Targeted expression of IGFBP3 demonstrates protective effects on vasculature and promotes repair following hyperoxic injury.
IGFBP3 may represent a physiological response to ischemia and a promising therapeutic target for ischemic diseases.